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Amoeba: a genus of protozoa in the order Nematopoda, suborder Nematopoda, and family Amoebidae. Transliteration of Amoeba. The insect is naked and soft, named after its ability to extend pseudopodia in various directions, resulting in an indeterminate body shape. Pseudo feet not only have the function of movement, but also can feed. It can be seen year-round in ponds, small ditches, and paddy fields. Amoebids can invade the bodies of humans and animals, causing diseases. The most common is amoeboid dysentery, which is the pathogen of human amoebic dysentery. China has discovered cases of human deaths caused by free living amoebas.
Due to different living environments, they can be divided into Entamoeba and free-living Amoeba. The former parasitizes humans and animals and mainly consists of four genera: Entamoeba, Endolimax, Iodamoeba, and Dientamoeba; The latter lives in water and soil, occasionally invading animal bodies, mainly consisting of five genera, namely Naegleria, Acanthamoeba, Hartmannella, Vablkampfia, and Sappinia.
Introduction
It is now known that the histolytic Entamoeba of the genus Entamoeba can cause amoebic dysentery and liver abscess, while the genera Negeri and Acanthamoeba mainly cause meningococcal amoebitis, keratitis, oral infections, and skin damage. In clinical practice, cases caused by Entamoeba histolytica are numerous, with a wide range of infections and significant harm. Free living amoebas exist in water, air, and soil around the world, which were previously believed to be unrelated to human disease.
After 1965, a type of amoebic meningitis was gradually discovered with a high mortality rate. There are two types of human meningoencephalitis caused by pathogenic free-living amoebae: primary amoebic meningoencephalitis (PAM) caused by Naegleria amoebae and granulomatous amoebic encephalitis (GAE) caused by Acanthamoeba.
life history
Free living amoebas live in water, soil, or decaying organic matter, with bacteria as the main nutrient body. They proliferate through binary division and can form cysts. The amoeboid type of N. Fowler can form cysts, but the flagellar type cannot.
Fukushi Nagri Amoeba is thermophilic, and its trophozoites grow best at 37-45 ℃ and die rapidly at 0-4 ℃. The cyst has strong resistance and remains active for 8 months at 51-65 ℃, and can survive for more than 4 months at -20 ℃. The cyst can also tolerate high concentrations of free chlorine
pathogenicity
When people swim in rivers, lakes, and ponds or wash their noses with epidemic water, amoebas containing Nagri enter the nasal cavity, proliferate, pass through the nasal mucosa and sieve plate, and travel along the olfactory nerve
Brain tissue infected with amoeba observed under a microscope
Brain tissue infected with amoeba observed under a microscope
Enters the brain, invades the central nervous system (CNS), and causes primary amoebic meningoencephalitis (PAM). Its invasiveness may be mainly due to the production of toxins or cytolytic substances that enhance phagocytic activity, and the surface phospholipase A and lysosomal enzymes of the parasite promote disease onset. Primary amoebic meningitis has a sudden onset and rapid progression of the condition. Symptoms such as headache, fever, and vomiting begin to appear, quickly leading to delirium, paralysis, coma, and death within a week at the earliest.
The main manifestation of its damage is acute and extensive hemorrhagic necrotizing meningitis, with a large amount of trophozoites in the cerebrospinal fluid and lesion tissue. The host's susceptibility factors may include a lack of IgA, which weakens the mucosal defense function.
Acanthamoeba is more widely distributed and can often be found in respiratory secretions. The primary site of the lesion can cause inflammation and granulomas in the skin or eyes, lungs, stomach, intestines, and ears. In cases of host immune suppression or weakening, it may spread through the bloodstream to the central nervous system, leading to granulomatous amoebic encephalitis (GAE). Its damage is mostly chronic granulomatous lesions; Therefore, the course of the disease is relatively long, up to 18-120 days. A few cases have an acute course and die within 10-14 days. Neurological signs indicate focal unilateral damage, with severe focal necrosis and edema. The patient experiences headaches, fever, vomiting, neck stiffness, dizziness, drowsiness, mental confusion, ataxia, and eventually coma and death. But those that have not metastasized to the brain are generally not fatal, and a few can heal on their own.
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